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Resistance to inhibiting effect of dexamethasone in patients with endogenous depression
Author(s) -
Nuller J. L.,
Ostroumova M. N.
Publication year - 1980
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.1980.tb00576.x
Subject(s) - depression (economics) , dexamethasone , endogeny , endogenous depression , resistance (ecology) , psychology , medicine , psychiatry , clinical psychology , pharmacology , biology , economics , keynesian economics , ecology
Suppression of 11‐hydroxycorticosteroids (11‐OHCS) release with dexamethasone (0.5 mg) has been investigated in 52 patients with endogenous depression and also in normals and in patients with other mental diseases. The suppression was considerably less in depressives (‐19 ± 5 %) than in control groups (approx. ‐60 %). The dexamethasone test indices were normalized during remission. To elucidate mechanisms of the dexamethasone inhibiting effect, the influence of tryptophan, DOPA and benzodiazepines on the 11‐OHCS level and the degree of its suppression with dexamethasone have been studied. The data indicate a dual effect of serotonin on the regulation of the adrenal function: it stimulates CRF secretion and increases the inhibiting effect of corticosteroids on CRF release. It is suggested that during depression the negative feedback is disturbed in the system – brain monoamines‐glucocorticoids. The possible role of this impairment in depression pathogenesis is considered.